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- W1966297218 endingPage "229" @default.
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- W1966297218 abstract "•Tissue specificity of DNA repair is not well understood and is understudied. •TNR instability is ideal to study DNA repair in different tissues. •Chromatin, repair rates, and protein levels may account for this tissue specificity. •System-level experiments will improve understanding of tissue-specific DNA repair. DNA must constantly be repaired to maintain genome stability. Although it is clear that DNA repair reactions depend on cell type and developmental stage, we know surprisingly little about the mechanisms that underlie this tissue specificity. This is due, in part, to the lack of adequate study systems. This review discusses recent progress toward understanding the mechanism leading to varying rates of instability at expanded trinucleotide repeats (TNRs) in different tissues. Although they are not DNA lesions, TNRs are hotspots for genome instability because normal DNA repair activities cause changes in repeat length. The rates of expansions and contractions are readily detectable and depend on cell identity, making TNR instability a particularly convenient model system. A better understanding of this type of genome instability will provide a foundation for studying tissue-specific DNA repair more generally, which has implications in cancer and other diseases caused by mutations in the caretakers of the genome. DNA must constantly be repaired to maintain genome stability. Although it is clear that DNA repair reactions depend on cell type and developmental stage, we know surprisingly little about the mechanisms that underlie this tissue specificity. This is due, in part, to the lack of adequate study systems. This review discusses recent progress toward understanding the mechanism leading to varying rates of instability at expanded trinucleotide repeats (TNRs) in different tissues. Although they are not DNA lesions, TNRs are hotspots for genome instability because normal DNA repair activities cause changes in repeat length. The rates of expansions and contractions are readily detectable and depend on cell identity, making TNR instability a particularly convenient model system. A better understanding of this type of genome instability will provide a foundation for studying tissue-specific DNA repair more generally, which has implications in cancer and other diseases caused by mutations in the caretakers of the genome." @default.
- W1966297218 created "2016-06-24" @default.
- W1966297218 creator A5084217433 @default.
- W1966297218 date "2014-06-01" @default.
- W1966297218 modified "2023-10-16" @default.
- W1966297218 title "Tissue specificity in DNA repair: lessons from trinucleotide repeat instability" @default.
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